POST MORTEM DIAGNOSIS OF EARLY MYOCARDIAL INFARCTION.
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ABSTRACT:
SUBMITTER: Kotabagi RB
PROVIDER: S-EPMC5532002 | biostudies-other | 2000 Apr
REPOSITORIES: biostudies-other
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Project description:Bedrest and immobilization following a myocardial infarction (MI) can lead to functional impairment that can persist following hospitalization. Early mobilization (EM) is associated with good functional and clinical outcomes in critical care, medical and surgical settings. However, the impact and current role of EM in post-MI care has not been well-defined. Our objective was to assess the evidence for post-MI mobilization, define current post-MI mobilization practice, and understand perspectives of cardiovascular professionals toward mobilization. A scoping review related to "early mobilization" and "myocardial infarction" was performed using the Joanna Briggs Institute Methodology. Pubmed, Embase, Google Scholar, Cochrane Library and CINAHL databases were included. Results were categorized into six topic areas. There were 59 references included in the analysis. There was evidence for the effectiveness and safety of earlier mobilization in experimental studies of the pre-revascularization era, but there was a lack of strong evidence for EM in contemporary post-MI care. Mobilization appears to be safe following arterial catheterization and is associated with minimal hemodynamic and respiratory compromise. Most people are delayed in mobilizing post-MI and spend the majority of the initial hospitalization period lying in bed. Only 1 of 7 current major cardiovascular professional societies guidelines recommend EM post-MI. There were no studies exploring the perspectives of cardiovascular professionals toward mobilization. EM may be beneficial in the post-MI care. However, there is an evidence gap for the impact of EM post-MI in the contemporary literature. More robust evidence from randomized clinical trials is required to inform clinicians and influence practice.
| S-EPMC7430744 | biostudies-literature
Project description:PURPOSE:Exercise-induced skeletal muscle deoxygenation is startling by its absence in early post-myocardial infarction (MI) patients. Exercise training early post-MI is associated with reduced cardiovascular risk and increased aerobic capacity. We therefore investigated whether aerobic training could enhance the muscle deoxygenation in early post-MI patients. METHODS:21 ± 8 days after the first MI patients (n = 16) were divided into 12-week aerobic training (TR, n = 10) or non-training (CON, n = 6) groups. Before and after intervention, patients performed ramp bicycle exercise until exhaustion. Muscle deoxygenation was measured at vastus lateralis by near-infrared spectroscopy during exercise. RESULTS:Aerobic training significantly increased peak oxygen uptake (VO2) (18.1 ± 3.0 vs. 22.9 ± 2.8 mL/kg/min), decreased the change in muscle oxygen saturation from rest to submaximal and peak exercise (?SmO2; 2.4 ± 5.7 vs. -7.0 ± 3.4 %), and increased the relative change in deoxygenated hemoglobin/myoglobin concentration from rest to submaximal (-1.5 ± 2.3 vs. 3.0 ± 3.6 ?mol/L) and peak exercise (1.1 ± 4.5 vs. 8.2 ± 3.5 ?mol/L). Change in total hemoglobin/myoglobin concentration in muscle was not significantly affected by training. In CON, no significant alterations were found after 12 weeks in either muscle deoxygenation or peak VO2 (18.6 ± 3.8 vs. 18.9 ± 4.6 mL/kg/min). An increase in peak VO2 was significantly negatively correlated with change in ?SmO2 (r = -0.65) and positively associated with change in ?deoxy-Hb/Mb at peak exercise (r = 0.64) in TR. CONCLUSIONS:In early post-MI patients, aerobic training enhanced skeletal muscle deoxygenation, and the enhancement was related to increased aerobic capacity.
| S-EPMC4819748 | biostudies-other
Project description:ObjectiveThere is a clinical need for early and accurate diagnosis of acute myocardial infarction (AMI). Current European Society of Cardiology (ESC) guidelines recommend diagnosis of non-ST-elevation AMI based on serial troponin measurements. We aimed to challenge the ESC guidelines using 1) a high-sensitivity troponin I (hs-TnI) baseline cutoff, 2) an absolute hs-TnI change after 1 hour and 3) additional application of an ischemic ECG.Methods1,516 patients with suspected AMI presenting to the emergency department were included. Hs-TnI was measured directly at admission, after 1 and 3 hours. We investigated baseline concentrations, absolute changes of hs-TnI and additional application of an ischemic ECG to diagnose AMI. A positive predictive value (PPV) of more than 85% was targeted.ResultsThe median age of the study population was 65 years; 291 patients were diagnosed with AMI. The PPV of the 3-hours ESC algorithm was 85.5% (CI 79.7, 90.1) and 65.8% (CI 60.5,70.8) for the 1-hour algorithm. Using a high baseline hs-TnI concentration of 150 ng/L resulted in a PPV of 87.8% (CI 80.9,92.9). Alternatively, a hs-TnI change of 20 ng/L after 1 hour, resulted in a PPV of 86.5% (80.9,91.0), respectively for the diagnosis of AMI. Additional use of an ischemic ECG increased the PPV to 90.5% (CI 83.2,95.3), while reducing the efficacy.ConclusionThe diagnosis of AMI based on hs-TnI is challenging. The application of absolute hs-TnI changes after 1 hour may facilitate rapid rule-in of patients.Trial registrationwww.clinicaltrials.gov (NCT02355457).
| S-EPMC5363912 | biostudies-literature
Project description: Not available
| S-EPMC7451908 | biostudies-literature
Project description:Highlights•The mechanical complications of acute myocardial infarction (AMI) can be catastrophic.•A Gerbode type defect after AMI is rare.•Surgery is the mainstay of treatment, but percutaneous options are available.•Gerbode defects can be congenital or acquired and can be closed percutaneously.•Echocardiography reliably evaluates the mechanical complications of AMI.
| S-EPMC6034478 | biostudies-other
Project description:Background We aimed to understand the characteristics and outcomes of patients readmitted with a recurrent myocardial infarction (RMI) within 90 days of discharge after an acute myocardial infarction (early RMI). Methods and Results We analyzed the timing of reinfarction, etiology, and outcome for all patients admitted with an early RMI within 90 days of discharge after an acute myocardial infarction between January 1, 2010 and January 1, 2017. We identified 6626 admissions for acute myocardial infarction (index myocardial infarction) which led to 168 cases of RMI within 90 days of discharge. The mean patient age was 65.1±13.1 years, and 37% were women. The 90-day probability of readmission with an early RMI was 2.5%. Black race, medical management, higher troponin T, and shorter length of stay were independent predictors of early RMI. Medically managed group had a higher risk for early RMI compared with percutaneous coronary intervention (P=0.04) or coronary artery bypass grafting (P=0.2). Predominant mechanisms for reinfarction were stent thrombosis (17%), disease progression (12%), and unchanged coronary artery disease (11%). At 5 years, the all-cause mortality rate for patients with an early RMI was 49% (95% CI, 40%-57%) compared with 22% (95% CI, 21%-23%) for patients without an early RMI (P<0.0001). Conclusions Early RMI is a life-threatening condition with nearly 50% mortality within 5 years. Stent-related events and progression in coronary artery disease account for most early RMI. Medication compliance, aggressive risk factor management, and care transitions should be the cornerstone in preventing early RMI.
| S-EPMC8475017 | biostudies-literature
Project description:Hybrid PET/MR imaging is an emerging imaging modality combining positron emission tomography (PET) and magnetic resonance imaging (MRI) in the same system. Since the introduction of clinical PET/MRI in 2011, it has had some impact (e.g., imaging the components of inflammation in myocardial infarction), but its role could be much greater. Many opportunities remain unexplored and will be highlighted in this review. The inflammatory process post-myocardial infarction has many facets at a cellular level which may affect the outcome of the patient, specifically the effects on adverse left ventricular remodeling, and ultimately prognosis. The goal of inflammation imaging is to track the process non-invasively and quantitatively to determine the best therapeutic options for intervention and to monitor those therapies. While PET and MRI, acquired separately, can image aspects of inflammation, hybrid PET/MRI has the potential to advance imaging of myocardial inflammation. This review contains a description of hybrid PET/MRI, its application to inflammation imaging in myocardial infarction and the challenges, constraints, and opportunities in designing data collection protocols. Finally, this review explores opportunities in PET/MRI: improved registration, partial volume correction, machine learning, new approaches in the development of PET and MRI pulse sequences, and the use of novel injection strategies.
| S-EPMC7391987 | biostudies-literature
Project description:Even in the era of percutaneous reperfusion therapy, left ventricular (LV) remodeling after myocardial infarction (MI) leading to heart failure remains a major health concern. Contractile dysfunction of the infarcted myocardium results in an increased pressure load, leading to maladaptive reshaping of the LV. Several percutaneous transcatheter procedures have been developed to deliver devices that restore LV shape and function. The purposes of this review are to discuss the spectrum of transcatheter devices that are available or in development for attenuation of adverse LV remodeling and to critically examine the available evidence for improvement of functional status and cardiovascular outcomes.
| S-EPMC6208878 | biostudies-literature
Project description:Matrix metalloproteinase-9 (MMP-9) is robustly elevated in the first week post-myocardial infarction (MI). Targeted deletion of the MMP-9 gene attenuates cardiac remodeling post-MI by reducing macrophage infiltration and collagen accumulation through increased apoptosis and reduced inflammation. In this study, we used a translational experimental design to determine whether selective MMP-9 inhibition early post-MI would be an effective therapeutic strategy in mice. We enrolled male C57BL/6J mice (3-6months old, n=116) for this study. Mice were subjected to coronary artery ligation. Saline or MMP-9 inhibitor (MMP-9i; 0.03?g/day) treatment was initiated at 3h post-MI and the mice were sacrificed at day (D) 1 or 7 post-MI. MMP-9i reduced MMP-9 activity by 31±1% at D1 post-MI (p<0.05 vs saline) and did not affect survival or infarct area. Surprisingly, MMP-9i treatment increased infarct wall thinning and worsened cardiac function at D7 post-MI. While MMP-9i enhanced neutrophil infiltration at D1 and macrophage infiltration at D7 post-MI, CD36 levels were lower in MMP-9i compared to saline, signifying reduced phagocytic potential per macrophage. Escalation and prolongation of the inflammatory response at D7 post-MI in the MMP-9i group was evident by increased expression of 18 pro-inflammatory cytokines (all p<0.05). MMP-9i reduced cleaved caspase 3 levels at D7 post-MI, consistent with reduced apoptosis and defective inflammation resolution. Because MMP-9i effects on inflammatory cells were significantly different from previously observed MMP-9 null mechanisms, we evaluated pre-MI (baseline) systemic differences between C57BL/6J and MMP-9 null plasma. By mass spectrometry, 34 plasma proteins were significantly different between groups, revealing a previously unappreciated altered baseline environment pre-MI when MMP-9 was deleted. In conclusion, early MMP-9 inhibition delayed inflammation resolution and exacerbated cardiac dysfunction, highlighting the importance of using translational approaches in mice.
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Project description:BackgroundAcute kidney injury (AKI) is a common complication of acute myocardial infarction (AMI), and is associated with adverse outcomes. The study aimed to identify a miRNA signature for the early diagnosis of post-AMI AKI.MethodsA total of 108 patients admitted to a coronary care unit (CCU) were divided into four subgroups: AMI-AKI-, AMI+AKI-, AMI+AKI+, and AMI-AKI+. Thirty-six miRNA candidates were selected based on an extensive literature review. Real-time quantitative RT-PCR analysis was used to determine the expression levels of these miRNAs in the serum collected on the day of CCU admittance. TargetScan 7.1 and miRDB databases were used for target prediction and Metacore 6.13 was used for pathway analysis.ResultsThrough a stepwise selection based on abundance, hemolytic effect and differential expression between four groups, 9 miRNAs were found to have significantly differential expression levels as potential biomarkers for post-AMI AKI specifically. Noticeably, the expression levels of miR-24, miR-23a and miR-145 were significantly down-regulated in AMI+AKI+ patients compared to those in AMI+AKI- patients. Combination of the three miRNAs as a panel showed the best performance in the early detection of AKI following AMI (AUC = 0.853, sensitivity 95.65%), compared to the analysis of serum neutrophil gelatinase-associated lipocalin (AUC = 0.735, sensitivity 63.16%). Furthermore, bioinformatic analysis indicated that these three miRNAs regulate the transforming growth factor beta signaling pathway and involve in apoptosis and fibrosis in AKI.ConclusionsFor the first time, this study identify a unique circulating miRNA signature (miR-24-3p, miR-23a-3p, miR-145-5p) that can potentially early detect AKI following AMI and may be involved in renal injury and fibrosis in post-AMI AKI pathogenesis.
| S-EPMC6492315 | biostudies-literature